Medd et al.,1 retrospectively studied the occurrence of paraproteinaemia after allo-SCT in a cohort of 91 patients. They detected a paraproteinaemia incidence of 32%, multiple in the majority of cases, with a predominance of an IgG isotype and with equal kappa/lambda restriction. In this report, the most important risk factor for the development of post-transplant paraproteinaemia was CMV reactivation, which was more frequent when alemtuzumab was included in conditioning regimen. The authors also described a poorer OS in patients with paraproteinaemia, with relapse being the commonest cause of death in this group of patients. None of the patients with paraproteinaemia subsequently developed myeloma or a lymphoproliferative disorder and only one patient developed cryoglobulinemia. In this study, EBV reactivation was not monitored. Babel et al.2 first reported the association between the occurrence of paraproteinaemia and EBV reactivation after renal transplantation. Since then, paraproteinaemia has been largely reported in solid organ transplant recipients reactivating EBV.3, 4, 5, 6 More recently, we reported the association between EBV reactivation after SCT and the occurrence of abnormalities in γ-region at serum protein electrophoresis (SPE) in a cohort of 79 patients.7 EBV reactivation was detected in 49/79 patients (62%), 43 of them show asymptomatic EBV-DNAemia, whereas the other 6 patients progressed to EBV-related post-transplant lymphoproliferative disease. The global incidence of abnormalities in γ-region at SPE after allo-SCT in patients with EBV reactivation was 65.3% (32/49 patients), whereas it was 37.5% (9/24 evaluable) in patients who did not present viral reactivation (P=0.02). Paraproteinaemia after HSCT was identified in 23/28 evaluable patients (82%) with EBV reactivation and in 4/7 evaluable patients (57%) without viral reactivation, with a median level of 1.8 g/dL (range 0.07–3.5 g/dL). CMV reactivation was co-present in 17/49 patients, 13 of them with abnormalities in γ-region at SPE and 9/13 with also a paraproteinaemia. Considering that alemtuzumab, adopted by Medd et al.1 as GVHD prophylaxis in the series of patients with paraproteinemia, is considered as a risk factor for EBV reactivation after allogenic SCT, the role of CMV reactivation per se as a risk factor for the subsequent development of paraproteinemia should be kept with caution in the absence of EBV viral load monitoring.8, 9 In our series, pre-emptive therapy for EBV reactivation was able to modify the extent of paraproteinemia leading to complete disappearance of gammopathy in a significant number of patients and it calls for a causative effect. We propose that EBV reactivation evaluation should be carried out in patients submitted to allogeneic SCT as recommended by European Conference of Infections in Leukemia,10 particularly when recognized risk factors are present. Medd et al.1 did not perform an EBV load monitoring in patients after HSCT, and they reported that there is no evidence of progression to lymphoproliferative disorder in patients with paraproteinaemia after HSCT. In our cohort, 5/6 patients with post-transplant lymphoproliferative disease showed a paraproteinaemia and in 2 cases it persisted also after EBV clearance after Rituximab therapy. In contrast to that reported by Medd et al., in our experience no significant difference in OS of patients with EBV reactivation was seen between patients with or without paraproteinaemia.
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May 23, 2014
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